title: [Changes of leptin, tumor necrosis factor-alpha, neuropeptide Y levels and their association with insulin resistance and insulin secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees].
abstract: This investigation was made in regard to the changes of plasma Leptin, Tumor Necrosis Factor-alpha (TNF-alpha) and Neuropeptide Y (NPY) levels and their association with insulin resistance and beta-cell secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees in Chengdu area. Levels of Leptin, TNF-alpha, NPY and lipids (TG, TC, HDL-C) were determined in 86 type 2 diabetic mellitus (DM) patients, 73 normal glucose tolerant (NGT) first-degree relatives in familial type 2 diabetic pedigrees and 65 normal controls (NC) from non-diabetic families. All of the subjects underwent 75 g oral glucose tolerance test (OGTT). Plasma glucose, immunoreactive insulin (IRI) and true insulin (TI) levels were also determined. Fasting glucose and TI levels were used to calculate homeostasis model assessment-insulin resistance (HOMA-IR) and HOMA-beta cell indexes. After being adjusted for age and body mass index (BMI), the levels of Leptin in DM and NGT first-degree relatives were all significantly higher than that in normal controls (P < 0.05). Type 2 diabetic patients showed significantly elevated TNF-alpha levels than did the normal controls (P < 0.05). Furthermore, diabetic subjects showed significantly higher HOMA-IR and lower HOMA-B levels, compared with those in NGT and NC groups (P < 0.05). No statistically significant difference was found in regard to NPY among three groups. NGT first-degree relatives showed significantly higher levels of TG, fasting IRI, OGTT-2h IRI and HOMA-IR than did the normal controls (P < 0.05). Leptin was positively correlated with age, BMI, waist, A1c, fasting and OGTT-2h glucose, OGTT-2h TI and TNF-alpha in all subjects, and was negatively correlated with HOMA-B in females. Leptin levels were significantly elevated in NGT first-degree relatives, which implied that genetic defects of Leptin may play a role in the development of familial type 2 diabetic pedigrees.
authors.affiliation: Division of Endocrinology and Metabolism, West China Hospital of Sichuan University, Chengdu 610041, China. renyan22@yahoo.com.cn
authors.forename: Yan
authors.initials: Y
authors.lastname: Ren
authors.forename: Xiujun
authors.initials: X
authors.lastname: Li
authors.forename: Haoming
authors.initials: H
authors.lastname: Tian
authors.forename: Jinzhong
authors.initials: J
authors.lastname: Liang
authors.forename: Xiangxun
authors.initials: X
authors.lastname: Zhang
authors.forename: Honglin
authors.initials: H
authors.lastname: Yu
authors.forename: Jianan
authors.initials: J
authors.lastname: Wang
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000235:genetics*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009478:Neuropeptide Y / Q000097:blood*; D010375:Pedigree; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D007328:Insulin; D020738:Leptin; D009478:Neuropeptide Y; D014409:Tumor Necrosis Factor-alpha